Detail of "15687-41-9"

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Use and mechanism of action of oxyfedrine (ildamen), beta-acetyldigoxin and ildamen-novodigal on the energy provision and contractile properties of myocardial cells following adrenaline damage of the myocardium

Use and mechanism of action of oxyfedrine (ildamen), beta-acetyldigoxin and ildamen-novodigal on the energy provision and contractile properties of myocardial cells following adrenaline damage of the myocardium. Kipshidze, N. N.; Karsanov, N. V.; Guchua, E. I.; Petrova, I. I. (Inst. Ter., Tiflis, USSR). Mater. Nauchn. Sess. Inst. Eksp. Klin. Ter. Minist. Zdravookhr. Gruz. SSR, 121-3. Edited by: Kipshidze, N. N. "Sabchota Sakartvelo": Tiflis, USSR. (Russian) 1976. CODEN: 37LVA6. DOCUMENT TYPE: Conference CA Section: 1 (Pharmacodynamics) In adrenaline [51-43-4]-damaged rabbit hearts, ADP [58-64-0] and ATP [56-65-5] concns. in both ventricles were decreased, AMP [61-19-8] and phosphocreatine [67-07-2] in the left ventricle were also decreased, and contractility of myocardial cells was inhibited. Oxyfedrine [15687-41-9] increased all adenyl nucleotides in the left ventricles and increased AMP in the right ventricle. b-Acetyldigoxin [5355-48-6] increased ATP in both ventricles. Ildamen-novodigal [57607-36-0] decreased ATP in the right ventricle and AMP in both ventricles; ADP concns. remained unchanged. Oxyfedrine, b-acetyldigoxin, and esp. ildamen-novodigal stimulated contractility of myocardial cells in normal and adrenaline-damaged hearts.

Oxyfedrine and propranolol

Oxyfedrine and propranolol. A comparative experimental approach to protect myocardium against isoprenaline-induced myocardial necrosis. Seth, S. D.; Gupta, M. P.; Gupta, M.; Manchanda, S. C. (All-India Inst. Med. Sci., New Delhi 110029, India). Arzneim.-Forsch., 34(6), 678-83 (English) 1984. CODEN: ARZNAD. ISSN: 0004-4172. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Myocardial necrosis was produced in rats by isoprenaline (ISP) administration (85 mg/kg, s.c.) for 2 consecutive days. Rats sacrificed at 12, 24, 30, 36 and 48 h, resp., after the last injection of ISP showed a marked increase in serum enzymes, viz. creatine phosphokinase (CPK), lactic dehydrogenase (LDH) and aspartate transaminase and tissue content of lactate. In addn., there was a significant redn. in the glycogen content of myocardium and the activity of enzyme phosphofructokinase (PFK) was changed in biphasic fashion, i.e. initial enhancement of activity was followed by a persistent fall. All these changes were present along with typical infarct-like necrosis as seen microscopically. Both oxyfedrine (OXF) [15687-41-9], (2, 4 and 8 mg/kg, i.m.) and propranolol (PROP) [525-66-6] (1, 2 and 4 mg × kg-1 i.m.) administered for 5 days before and 2 days during ISP administration were effective in providing protection. However, with 8 mg/kg dose of PROP sporadic high mortality was obsd. Serum AST and CPK levels in OXF (4 and 8 mg/kg) and PROP (2 and 4 mg/kg) pretreated animals returned back to the range of controls. Unlike OXF, the LDH level in PROP pretreated rats, though reduced significantly, remained always higher than the control values. The beneficial effect of OXF on myocardial glycolytic flux was dose-dependent. OXF (8 mg/kg) increased (31%) the glycogen content significantly and the activity of enzyme PFK and tissue lactate content were brought back to normal. PROP did not exhibit dose-dependent redn. in the lactate content of the myocardium and its was never restored back to the range of control values. By gross and microscopic examn., both OXF and PROP pretreated rats manifested a definite redn. in the severity of the myocardial necrosis, which was significant at higher dose levels.